Differential maturation of avidity of IgG antibodies to gp41, p24 and p17 following infection with HIV-1.

We have evaluated solid-phase ELISA IgG antibody avidity studies as a means of identifying cases of recent HIV-1 infection. Although separate studies on the avidity of anti-gp41 and anti-p24 antibodies in seroconvertors have been reported, a comparison of the ability of patients to simultaneously mature their immune response to more than one HIV antigen immediately following seroconversion appears to be lacking. We have demonstrated a maturation in anti-gp41 avidity which reflects the time since seroconversion in all cases. In contrast, however, only some patients produced high-avidity anti-p24 or anti-p17 antibodies during the same time span. While the avidity of anti-gp41 antibodies remained high in cases of non-recent HIV infection, even in the face of advanced disease, we have confirmed the findings of others that the avidity of anti-p24 falls before the onset of ARC or AIDS. Therefore, whilst the avidity of anti-gp41 antibodies could reliably be of value in identifying cases of recent HIV infection, the avidity of anti-p24 or anti-p17 antibodies could not, but may be of prognostic value, even at an early stage. The time taken to reach maximum anti-p17, anti-p24 and anti-gp41 titres was variable, but anti-gp41 titres, like anti-gp41 avidity, remained high. In contrast, anti-p24 titres fell, even during the early followup period in some seroconvertors. Anti-p24 antibody avidity, however, appeared to be a better predictor of disease progression in 'remote' cases than anti-p24 titre. The avidity and titres of these antibodies are presented in relation to the clinical details, p24 antigen status, CD4 and CD8 counts where these are known.

Identification of pregnancies at risk from cytomegalovirus infection.

The fluorescent antibody technique was used for the identification of specific cytomegalovirus IgM in the sera of twenty-four of 1065 unmarried pregnant women. Seventeen of them were followed to term and five infected infants were identified. Two other infants had CMV IgM in neonatal serum samples but virus excretion was not demonstrated. The congenital infection rate in this study was 5.3 per 1000 births by virus excretion and 7.9 per 1000 if cases with specific IgM are included; from previous studies a rate of 8.8 per 1000 was expected. The reasons for the lack of relationship between specific IgM in the mothers' serum and infected babies is discussed.